SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Tretli Steinar) "

Sökning: WFRF:(Tretli Steinar)

  • Resultat 1-10 av 68
  • [1]234567Nästa
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Hemminki, Kari, et al. (författare)
  • Familial risks in nervous-system tumours: a histology-specific analysis from Sweden and Norway
  • 2009
  • Ingår i: The Lancet Oncology. - Elsevier. - 1474-5488. ; 10:5, s. 481-488
  • Tidskriftsartikel (refereegranskat)abstract
    • Background There are limited data available on tumour subtype-specific familial risks for nervous-system tumours. We aimed to provide such data at the population level. Methods We used data from the nationwide Swedish and Norwegian databases on familial cancer to calculate standardised incidence ratios (SIRS) for the familial risk of developing a nervous-system tumour in offspring born after 1931 (Sweden) or 1900 (Norway) whose parents or siblings were probands. Findings 54195 patients had nervous-system tumours, 22331 of whom belonged to the offspring generation aged 0-72 years in Sweden and 0-51 years in Norway. Of 709 familial patients in the offspring generation, 438 (61.8%) had a parent affected by a nervous-system tumour (SIR 1.66; 95% CI 1.51-1.82), 236 (33.3%) had a sibling affected by a nervous-system tumour (SIR 2.01; 95% CI 1.76-2.28), and 35 (4.9%) belonged to families with a parent and at least two siblings affected by a nervous-system tumour (multiplex families; SIR 13.40; 95% CI 9.33-18.66). The SIR for glioma was 1.8 (1.5-2.0) when a parent was a proband, but increased to 11.2 (5.7-19.5) in multiplex families. Early-onset neurinoma and haemangioma showed high familial risks; with an SIR for neurinoma of 1.7 (1.4-2.2) for offspring of affected parents, 2.7 (2.0-3.5) for siblings, and 27.2 (13.5-48.8) for multiplex families, and an SIR for haemangioma of 2.4 (1.4-3.8) for offspring of affected parents. Histology-specific population-based familial risks were shown for meningioma (1.6 for offspring of affected parents; 95% CI 1.3-2.0), ependymoma (2.7 for young offspring <20 years; 1.1-5.5), medulloblastoma (4.1 for siblings; 1.7-8.1), and neuroblastoma (3.2 for siblings; 1.1-6.9). Interpretation Our results suggest a complex genetic background for nervous-system tumours, which differs depending on the age of onset and histological subtype of the tumour. High sibling risks might suggest recessive inheritance. As the high-penetrant multiplex families only accounted for about 5% of familial nervous-system tumours, most familial cases are probably caused by low-penetrance genes.
  •  
2.
  • Akre, Olof, et al. (författare)
  • Epstein-Barr virus and cytomegalovirus in relation to testicular-cancer risk : a nested case-control study
  • 1999
  • Ingår i: International Journal of Cancer. - 0020-7136 .- 1097-0215. ; 82:1, s. 1-5
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>An infectious etiology of testicular cancer has been suggested. We have evaluated seroreactivity against cytomegalovirus (CMV) and Epstein-Barr virus (EBV) in relation to testicular-cancer risk in a case-control study, nested within a cohort of prospectively collected serum specimens from 293,692 individuals. For each of 81 cases of testicular cancer identified, 3 controls were randomly selected from the cohort. Serum IgG antibody titers against CMV and EBV were determined using enzyme-linked immunosorbent assays (ELISAs) and immunofluorescence methods. Odds ratios (OR) were obtained from conditional logistic-regression models. No association was found between CMV positivity and testicular cancer overall (OR = 1.08; 95% confidence interval 0.60-1.94); risk for testicular seminoma was increased among CMV seropositive [OR = 1.70 (0.80-3.59)], whereas seropositivity was associated with decreased risk for testicular non-seminoma [OR = 0.54 (0.19-1.56)] (p for heterogeneity, 0.09). For EBV, the risk for testicular cancer was increased among individuals seropositive for viral capsid antigen (VCA) [OR = 2.74 (0.62-12.12)]. The results lend some support to the hypothesis of an infectious etiology, and we propose that future studies should take into account age at infection.</p>
  •  
3.
  • Almquist, Martin, et al. (författare)
  • Metabolic factors and risk of thyroid cancer in the Metabolic syndrome and Cancer project (Me-Can).
  • 2011
  • Ingår i: Cancer Causes and Control. - Springer. - 1573-7225. ; 22, s. 743-751
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To investigate metabolic factors and their possible impact on risk of thyroid cancer. METHODS: A prospective cohort study was conducted based on seven population-based cohorts in Norway, Austria, and Sweden, in the Metabolic syndrome and Cancer project (Me-Can). Altogether 578,700 men and women with a mean age of 44.0 years at baseline were followed for on average 12.0 years. Relative risk of incident thyroid cancer was assessed by levels of BMI, blood pressure, and blood levels of glucose, cholesterol, triglycerides, and by a combined metabolic syndrome (MetS) score. Risk estimates were investigated for quintiles, and a z score distribution of exposures was analyzed using Cox proportional hazards regression. RESULTS: During follow-up, 255 women and 133 men were diagnosed with thyroid cancer. In women, there was an inverse association between glucose and thyroid cancer risk, with adjusted RR: 95% CI was 0.61 (0.41-0.90), p trend = 0.02 in the fifth versus the first quintile, and a positive association between BMI and thyroid cancer risk with a significant trend over quintiles. There was no association between the other metabolic factors, single or combined (Met-S), and thyroid cancer. CONCLUSION: In women, BMI was positively, while blood glucose levels were inversely, associated with thyroid cancer.
  •  
4.
  • Almquist, Martin, et al. (författare)
  • Metabolic factors and risk of thyroid cancer in the Metabolic syndrome and Cancer project (Me-Can)
  • 2011
  • Ingår i: Cancer Causes and Control. - Springer. - 0957-5243 .- 1573-7225. ; 22:5, s. 743-751
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Objective  To investigate metabolic factors and their possible impact on risk of thyroid cancer. Methods  A prospective cohort study was conducted based on seven population-based cohorts in Norway, Austria, and Sweden, in the Metabolic syndrome and Cancer project (Me-Can). Altogether 578,700 men and women with a mean age of 44.0 years at baseline were followed for on average 12.0 years. Relative risk of incident thyroid cancer was assessed by levels of BMI, blood pressure, and blood levels of glucose, cholesterol, triglycerides, and by a combined metabolic syndrome (MetS) score. Risk estimates were investigated for quintiles, and a <em>z</em> score distribution of exposures was analyzed using Cox proportional hazards regression. Results  During follow-up, 255 women and 133 men were diagnosed with thyroid cancer. In women, there was an inverse association between glucose and thyroid cancer risk, with adjusted RR: 95% CI was 0.61 (0.41–0.90), <em>p</em> trend = 0.02 in the fifth versus the first quintile, and a positive association between BMI and thyroid cancer risk with a significant trend over quintiles. There was no association between the other metabolic factors, single or combined (Met-S), and thyroid cancer. Conclusion  In women, BMI was positively, while blood glucose levels were inversely, associated with thyroid cancer.</p>
  •  
5.
  • Bjorge, Tone, et al. (författare)
  • Metabolic Syndrome and Breast Cancer in the Me-Can (Metabolic Syndrome and Cancer) Project
  • 2010
  • Ingår i: Cancer Epidemiology Biomarkers & Prevention. - American Association for Cancer Research. - 1538-7755. ; 19:7, s. 1737-1745
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Few studies have assessed the metabolic syndrome (MetS) as an entity in relation to breast cancer risk, and results have been inconsistent. We aimed to examine the association between MetS factors (individually and combined) and risk of breast cancer incidence and mortality. Methods: Two hundred ninety thousand women from Austria, Norway, and Sweden were enrolled during 1974-2005, with measurements of height, weight, blood pressure, and levels of glucose, cholesterol, and triglycerides. Relative risks (RR) of breast cancer were estimated using Cox proportional hazards regression for each MetS factor in quintiles and for standardized levels (z-scores) and for a composite z-score for the MetS. Results: There were 4,862 incident cases of breast cancer and 633 deaths from breast cancer identified. In women below age 50, there was a decreased risk of incident cancer for the MetS (per 1-unit increment of z-score; RR, 0.83; 95% confidence interval, 0.76-0.90) as well as for the individual factors (except for glucose). The lowest risks were seen among the heaviest women. In women above age 60, there was an increased risk of breast cancer mortality for the MetS (RR, 1.23; 95% confidence interval, 1.04-1.45) and for blood pressure and glucose. The strongest association with mortality was seen for increased glucose concentrations. Conclusions: The MetS was associated with a decreased risk of incident breast cancer in women below age 50 with high body mass index, and with an increased risk of breast cancer mortality in women above 60. Impact: Lifestyle interventions as recommended for cardiovascular disease prevention may be of value to prevent breast cancer mortality in postmenopausal women. Cancer Epidemiol Biomarkers Prev; 19(7); 1737-45. (C) 2010 AACR.
  •  
6.
  • Bjorge, Tone, et al. (författare)
  • Metabolic Syndrome and Endometrial Carcinoma
  • 2010
  • Ingår i: American Journal of Epidemiology. - Oxford University Press. - 0002-9262. ; 171:8, s. 892-902
  • Tidskriftsartikel (refereegranskat)abstract
    • The authors examined the association between the metabolic syndrome and risk of incident endometnal and fatal uterine corpus cancer within a large prospective cohort study Approximately 290,000 women from Austria, Norway, and Sweden were enrolled during 1974-2005, with measurements of height, weight, systolic and diastolic blood pressure, and circulating levels of glucose, total cholesterol, and tnglycendes Relative risks were estimated using Cox proportional hazards regression. The metabolic syndrome was assessed as a composite z score, as the standardized sum of z scores for body mass index, blood pressure, glucose, cholesterol, and tnglycendes. A total of 917 endonnetnal carcinomas and 129 fatal cancers were identified Increased risks of incident endometnal carcinoma and fatal uterine corpus cancer were seen for the metabolic syndrome factors combined, as well as for individual factors (except for cholesterol) The relative risk of endometnal carcinoma for the metabolic syndrome was 1.37 (95% confidence interval 1 28, 1 46) per 1-unit increment of z score The positive associations between metabolic syndrome factors (both individually and combined) and endometrial carcinoma were confined to the heaviest women. The association between the metabolic syndrome and endometnal carcinoma risk seems to go beyond the risk conferred by obesity alone, particularly in women with a high body mass index
  •  
7.
  • Bjørge, Tone, et al. (författare)
  • BMI and weight changes and risk of obesity-related cancers : a pooled European cohort study
  • 2019
  • Ingår i: International Journal of Epidemiology. - Oxford University Press. - 0300-5771 .- 1464-3685. ; 48:6, s. 1872-2885
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background: Obesity is an established risk factor for several cancers. Adult weight gain has been associated with increased cancer risk, but studies on timing and duration of adult weight gain are relatively scarce. We examined the impact of BMI (body mass index) and weight changes over time, as well as the timing and duration of excess weight, on obesity- and non-obesity-related cancers.</p><p>Methods: We pooled health data from six European cohorts and included 221 274 individuals with two or more height and weight measurements during 1972–2014. Several BMI and weight measures were constructed. Cancer cases were identified through linkage with national cancer registries. Hazard ratios (HRs) of cancer with 95% confidence intervals (CIs) were derived from time-dependent Cox-regression models.</p><p>Results: During follow-up, 27 881 cancer cases were diagnosed; 9761 were obesity-related. The HR of all obesity-related cancers increased with increasing BMI at first and last measurement, maximum BMI and longer duration of overweight (men only) and obesity. Participants who were overweight before age 40 years had an HR of obesity-related cancers of 1.16 (95% CI 1.02, 1.32) and 1.15 (95% CI 1.04, 1.27) in men and women, respectively, compared with those who were not overweight. The risk increase was particularly high for endometrial (70%), male renal-cell (58%) and male colon cancer (29%). No positive associations were seen for cancers not regarded as obesity-related.</p><p>Conclusions: Adult weight gain was associated with increased risk of several major cancers. The degree, timing and duration of overweight and obesity also seemed to be important. Preventing weight gain may reduce the cancer risk.</p>
  •  
8.
  • Bjørge, Tone, et al. (författare)
  • BMI and weight changes and risk of obesity-related cancers : a pooled European cohort study
  • 2019
  • Ingår i: International Journal of Epidemiology. - 0300-5771 .- 1464-3685. ; 48:6, s. 1872-1885
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>BACKGROUND:</strong> Obesity is an established risk factor for several cancers. Adult weight gain has been associated with increased cancer risk, but studies on timing and duration of adult weight gain are relatively scarce. We examined the impact of BMI (body mass index) and weight changes over time, as well as the timing and duration of excess weight, on obesity- and non-obesity-related cancers.</p><p><strong>METHODS:</strong> We pooled health data from six European cohorts and included 221 274 individuals with two or more height and weight measurements during 1972-2014. Several BMI and weight measures were constructed. Cancer cases were identified through linkage with national cancer registries. Hazard ratios (HRs) of cancer with 95% confidence intervals (CIs) were derived from time-dependent Cox-regression models.</p><p><strong>RESULTS:</strong> During follow-up, 27 881 cancer cases were diagnosed; 9761 were obesity-related. The HR of all obesity-related cancers increased with increasing BMI at first and last measurement, maximum BMI and longer duration of overweight (men only) and obesity. Participants who were overweight before age 40 years had an HR of obesity-related cancers of 1.16 (95% CI 1.02, 1.32) and 1.15 (95% CI 1.04, 1.27) in men and women, respectively, compared with those who were not overweight. The risk increase was particularly high for endometrial (70%), male renal-cell (58%) and male colon cancer (29%). No positive associations were seen for cancers not regarded as obesity-related.</p><p><strong>CONCLUSIONS:</strong> Adult weight gain was associated with increased risk of several major cancers. The degree, timing and duration of overweight and obesity also seemed to be important. Preventing weight gain may reduce the cancer risk.</p>
  •  
9.
  • Bjørge, Tone, et al. (författare)
  • BMI and weight changes and risk of obesity-related cancers : a pooled European cohort study
  • 2019
  • Ingår i: International Journal of Epidemiology. - Oxford University Press. - 1464-3685. ; 48:6, s. 1872-1885
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Obesity is an established risk factor for several cancers. Adult weight gain has been associated with increased cancer risk, but studies on timing and duration of adult weight gain are relatively scarce. We examined the impact of BMI (body mass index) and weight changes over time, as well as the timing and duration of excess weight, on obesity- and non-obesity-related cancers. METHODS: We pooled health data from six European cohorts and included 221 274 individuals with two or more height and weight measurements during 1972-2014. Several BMI and weight measures were constructed. Cancer cases were identified through linkage with national cancer registries. Hazard ratios (HRs) of cancer with 95% confidence intervals (CIs) were derived from time-dependent Cox-regression models. RESULTS: During follow-up, 27 881 cancer cases were diagnosed; 9761 were obesity-related. The HR of all obesity-related cancers increased with increasing BMI at first and last measurement, maximum BMI and longer duration of overweight (men only) and obesity. Participants who were overweight before age 40 years had an HR of obesity-related cancers of 1.16 (95% CI 1.02, 1.32) and 1.15 (95% CI 1.04, 1.27) in men and women, respectively, compared with those who were not overweight. The risk increase was particularly high for endometrial (70%), male renal-cell (58%) and male colon cancer (29%). No positive associations were seen for cancers not regarded as obesity-related. CONCLUSIONS: Adult weight gain was associated with increased risk of several major cancers. The degree, timing and duration of overweight and obesity also seemed to be important. Preventing weight gain may reduce the cancer risk.
  •  
10.
  • Bjørge, Tone, et al. (författare)
  • Metabolic risk factors and ovarian cancer in the Metabolic Syndrome and Cancer project.
  • 2011
  • Ingår i: International Journal of Epidemiology. - Oxford University Press. - 1464-3685. ; 40, s. 1667-1677
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: No studies have so far evaluated the impact of the metabolic syndrome (MetS) as an entity on ovarian cancer risk. The authors aimed to examine the association between factors in the MetS, individually and combined, and risk of ovarian cancer incidence and mortality. METHODS: Altogether, 290 000 women from Austria, Norway and Sweden were enrolled during 1974-2005, with measurements taken of height, weight, blood pressure and levels of glucose, cholesterol and triglycerides. Relative risks (RRs) of ovarian cancer were estimated using Cox regression for each MetS factor in quintiles and for standardized levels (z-scores), and for a composite z-score for the MetS. RRs were corrected for random error in measurements. RESULTS: During follow-up, 644 epithelial ovarian cancers and 388 deaths from ovarian cancer were identified. There was no overall association between MetS and ovarian cancer risk. Increasing levels of cholesterol [RR 1.52, 95% confidence interval (95% CI) 1.01-2.29, per 1-U increment of z-score] and blood pressure (RR 1.79, 95% CI 1.12-2.86) conferred, however, increased risks of mucinous and endometrioid tumours, respectively. In women below the age of 50 years, there was increased risk of ovarian cancer mortality for MetS (RR 1.52, 95% CI 1.00-2.30). Increasing levels of BMI (RR 1.17, 95% CI 1.01-1.37) conferred increased risk of ovarian cancer mortality in women above the age of 50 years. CONCLUSION: There was no overall association between MetS and ovarian cancer risk. However, increasing levels of cholesterol and blood pressure increased the risks of mucinous and endometrioid tumours, respectively. Increasing levels of BMI conferred an increased risk of ovarian cancer mortality in women above the age of 50 years.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 68
  • [1]234567Nästa
Åtkomst
fritt online (20)
Typ av publikation
tidskriftsartikel (67)
doktorsavhandling (1)
Typ av innehåll
refereegranskat (67)
övrigt vetenskapligt (1)
Författare/redaktör
Tretli, Steinar (67)
Manjer, Jonas, (56)
Engeland, Anders (55)
Ulmer, Hanno (54)
Stocks, Tanja, (54)
Nagel, Gabriele (48)
visa fler...
Selmer, Randi (47)
Concin, Hans (47)
Stattin, Pär, (41)
Björge, Tone (40)
Häggström, Christel, (36)
Jonsson, Håkan, (35)
Hallmans, Göran (30)
Almquist, Martin, (23)
Bjorge, Tone (20)
Johansen, Dorthe, (19)
Lindkvist, Björn (16)
Hallmans, Goran (15)
Jonsson, Hakan (15)
Lukanova, Annekatrin (14)
Stattin, Par (13)
Haggstrom, Christel, (11)
Rapp, Kilian (10)
Lang, Alois (7)
Hemminki, Kari, (5)
Lindkvist, Bjorn (5)
Ghaderi, Sara (5)
Ekbom, Anders (4)
Sundquist, Kristina, (4)
Fallah, Mahdi, (4)
Tryggvadottir, Laufe ... (4)
Diem, Guenter (4)
Pukkala, Eero, (4)
Rosendahl, Ann H., (3)
Gissler, Mika (3)
Adami, Hans Olov (3)
Olsen, Jörgen H (3)
Hallmans, Göran, 194 ... (3)
Grotmol, Tom (3)
Liedberg, Fredrik, (2)
Jahnson, Staffan, (2)
Ulmert, David, (2)
Stattin, Paer (2)
Van Hemelrijck, Miek ... (2)
Orho-Melander, Marju ... (2)
Kharazmi, Elham, (2)
Madanat-Harjuoja, La ... (2)
Strasak, Alexander, (2)
Glimelius, Ingrid, 1 ... (2)
Harlid, Sophia (2)
visa färre...
Lärosäte
Lunds universitet (29)
Umeå universitet (25)
Uppsala universitet (11)
Göteborgs universitet (4)
Örebro universitet (2)
Linköpings universitet (1)
visa fler...
Karolinska Institutet (1)
visa färre...
Språk
Engelska (68)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (67)

År

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy